Essential Hypertension Pathology Lecture

1. ESSENTIAL HYPERTENSION

2. Outline
Definition
Etiology
Pathogenesis
Clinical features
Diagnosis
Complications
Treatment

3. Definition
Sustained elevation of blood
pressure
◦ Systolic blood pressure  140 mm Hg
◦ Diastolic blood pressure  90 mm Hg

4. Peripheral resistance is determined by:
the calibre
total cross-sectional area of the resistance vessels (small arteries and
arterioles).
Factors that increase cardiac output or peripheral resistance therefore
increase blood pressure.

5. Types of hypertension
PRIMARY (ESSENTIAL)
oaccounts for 95% cases of HTN.
ono universally established cause known.
SECONDARY
oless common cause of HTN ( 5%).
osecondary to other potentially rectifiable
causes.

6. Clinical forms of hypertension
Benign
Systole <200mmHg
Diastole <120mmHg
Hyaline arteriosclerosis
Malignant
Systole >200mmHg
Diastole >120mmHg
Hyperplastic arteriosclerosis

7. Etiology
Essential hypertension
Multifactorial disease.
Unknown specific etiology and pathogenesis .

8. Predisposing factors
MODIFIABLE
stress
obesity
High salt intake
lack of Mg2+, K+
ethanol  dose
smoking
NON-MODIFIABLE
positive family history
insulin resistance
Age
Sex
defect of local vasomotor regulation

9. Pathogenesis
Specific mechanisms unknown.
Proposed mechanisms:
Genetic factors
Reduced sodium excretion
Environmental factors
Increased vascular resistance

10. Mechanisms of essential hypertension
 Genetic factors
This is evidenced by:
i. Familial aggregation
ii. Occurrence of hypertension in twins
iii. Identification of hypertension susceptible gene (angiotensinogen gene)

11. Mechanisms of essential hypertension
Reduced sodium excretion
The kidney plays a key role in long-term control of blood pressure
excretion of salt and water controls intravascular volume.

12. Mechanisms of essential hypertension
Gene defects in enzymes involved in aldosterone metabolism such as:
aldosterone synthase
11 beta-hydroxylase
17 alpha-hydroxylase
lead to increased aldosterone secretion.
This leads to increased sodium and water retention
hence increased plasma volume and blood pressure.

13. Mechanisms of essential hypertension

14. Complications
Mutations in genes encoding ENaC.
Increased distal tubular reabsorption of sodium induced by aldosterone.

15. Mechanisms of essential hypertension
 Environmental factors such as stress ,obesity and smoking modify the impact of genetic
determinants thus leading to hypertension.
 Increased vascular resistance.- due to vasoconstriction of small arteries and arterioles or
structural changes in vessel wall

16. Clinical manifestations
Frequently asymptomatic until severe and target organ disease has occurred
◦ Fatigue, reduced activity tolerance
◦ Dizziness
◦ Palpitations, angina
◦ Dyspnea

17. Complications
Cerebrovascular disease
Stroke
Retinal Damage
Hypertensive heart disease
 Nephrosclerosis

18. Complications

19. Complications
NORMAL RETINA HYPERTENSIVE RETINOPATHY

20. Complications
Hypertensive heart disease

21. Treatment
LIFESTYLE MODIFICATION
- Weight reduction
Dietary changes
 Sodium restriction
Limitation of alcohol intake
Regular physical activity
Avoidance of tobacco use
Stress management
ANTIHYPERTENSIVE DRUGS
• Diuretics
• Adrenergic inhibitors
• β - Adrenergic blockers
• ACE Inhibitors
• Calcium channel blockers

22. THE END
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